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-Follidrone increases angiogenesis 30-50% which in turn increases blood flow as well as oxygen and nutrient transport into muscle tissues.

-Follidrone imitates the effects of endurance training as well as making endurance training more effective. Use of Follidrone can lead to significant increases in treadmill performance (∼50%) and enhanced in situ muscle fatigue resistance (∼30%).

-Follidrone increases follistatin levels. Follistatin is an antagonist to myostatin which inhibits excessive muscle growth. A study has also shown that increased levels of follistatin leads to increased muscle mass. Follistatin is part of the inhibin-activin-follistatin axis. Follistatin is an Activin binding protein. In the tissues activin has a strong role in cellular proliferation, thereby making follistatin the safeguard against uncontrolled cellular proliferation and also allowing it to function as an instrument of cellular differentiation. Both of these roles are vital in tissue rebuilding and repair.
In addition, increased follistatin levels combined with a lack of myostatin DOUBLED MUSCLE GROWTH.

Study results regarding Follidrone ingredients

Animals with reduced myostatin

Follodrone decreases Myostatin levels 49%+ as well as increasing markers of muscle growth. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family that inhibits muscle differentiation and growth in the process known as myogenesis. Myostatin is produced primarily in skeletal muscle cells, circulates in the blood and acts on muscle tissue, by binding a cell-bound receptor called the activin type II receptor. Reductions in myostatin = increased muscle mass and strength.

Follidrone Increases strength dramatically and quickly.
Treatment for 7 days yielded a bilateral increase in hand strength of 7%, which was accompanied by a significant decrease (-49%) in myostatin.

In addition our internal testers reported serious strength gains including-
-100lb increase in Deadlift in 4 days
-20lbs per arm on DB incline press in 10 days.
-6 inch gain on vert jump to 53 inches.
-one user compared the strength increase to halotestin.
Increases in mass were also reported by our internal testers including 10lbs weight gain in 10 days with what appears to be 0 BF% increase.
Users have also been reporting significant physique changes. Harder, leaner, and overall larger.

All information provided by me is for research purpose only. I do not sell illegal compounds nor can I supply anyone with a source for raw materials.

Sarcopenia is a notable and debilitating age-associated condition. Flavonoids are known for their healthy effects and limited toxicity. The flavanol (-)-epicatechin (Epi) enhances exercise capacity in mice, and Epi-rich cocoa improves skeletal muscle structure in heart failure patients. (-)-Epicatechin may thus hold promise as treatment for sarcopenia. We examined changes in protein levels of molecular modulators of growth and differentiation in young vs. old, human and mouse skeletal muscle. We report the effects of Epi in mice and the results of an initial proof-of-concept trial in humans, where muscle strength and levels of modulators of muscle growth were measured. In mice, myostatin and senescence-associated β-galactosidase levels increase with aging, while those of follistatin and Myf5 decrease. (-)-Epicatechin decreases myostatin and β-galactosidase and increases levels of markers of muscle growth. In humans, myostatin and β-galactosidase increase with aging while follistatin, MyoD and myogenin decrease. Treatment for 7 days with (-)-epicatechin increases hand grip strength and the ratio of plasma follistatin/myostatin. In conclusion, aging has deleterious effects on modulators of muscle growth/differentiation, and the consumption of modest amounts of the flavanol (-)-epicatechin can partially reverse these changes. This flavanol warrants its comprehensive evaluation for the treatment of sarcopenia.

Epicatechin imitates the effects of endurance training as well as making endurance training more effective.
In a 2012 research study one group of mice ran daily on a tread mill for five weeks where as the control group did nothing.
At the end of five weeks all animals did nothing for 14 days.
Half the trained mice were given epicatechin twice a day and the other half were given water.At the end of the 14-day detraining period, the mice that had been given (-)-epicatechin had retained much of the condition they had built up previously. When the researchers got the animals to run to the point of exhaustion, the mice that had been given (-)-epicatechin were faster, were able to keep running for longer and therefore also covered a greater distance.
When the mice's muscles were examined researchers saw that epicatechin supplementation had prevented training induced changes in muscle fibers from disappearing during inactivity.

The lifespan of diabetic patients is 7-8 y shorter than that of the general population because of hyperglycemia-induced vascular complications and damage to other organs such as the liver and skeletal muscle. Here, we investigated the effects of epicatechin, one of the major flavonoids in cocoa, on health-promoting effects in obese diabetic (db/db) mice (0.25% in drinking water for 15 wk) and Drosophila melanogaster (0.01-8 mmol/L in diet). Dietary intake of epicatechin promoted survival in the diabetic mice (50% mortality in diabetic control group vs. 8.4% in epicatechin group after 15 wk of treatment), whereas blood pressure, blood glucose, food intake, and body weight gain were not significantly altered. Pathological analysis showed that epicatechin administration reduced the degeneration of aortic vessels and blunted fat deposition and hydropic degeneration in the liver caused by diabetes. Epicatechin treatment caused changes in diabetic mice that are associated with a healthier and longer lifespan, including improved skeletal muscle stress output, reduced systematic inflammation markers and serum LDL cholesterol, increased hepatic antioxidant glutathione concentration and total superoxide dismutase activity, decreased circulating insulin-like growth factor-1 (from 303 &plusmn; 21 mg/L in the diabetic control group to 189 &plusmn; 21 mg/L in the epicatechin-treated group), and improved AMP-activated protein kinase-α activity in the liver and skeletal muscle. Consistently, epicatechin (0.1-8 mmol/L) also promoted survival and increased mean lifespan of Drosophila. Therefore, epicatechin may be a novel food-derived, antiaging compound.

The consumption of moderate amounts of cocoa products has been associated with reductions in the incidence of cardiovascular diseases. In animal studies, the flavanol (-)-epicatechin (Epi) yields cardioprotection. The effects may be partly due to its capacity to stimulate endothelial nitric oxide synthase (eNOS). The sustained activation of eNOS, as observed with exercise, can serve as a trigger of muscle angiogenesis via the activation of vascular endothelial growth factor (VEGF)-related events. Experiments were pursued to examine the potential of Epi to stimulate myocardial angiogenesis and determine the effects that its combined use with exercise (Ex) may trigger. Hearts obtained from a previous study were used for this purpose. Animals received 1 mg/kg of Epi or water (vehicle) via oral gavage (twice daily). Epi and/or Ex (by treadmill) was provided for 15 days. Results indicate that Ex or Epi significantly stimulate myocardial angiogenesis by ~30% above control levels. The use of Epi-Ex lead to further significant increases (to ~50%). Effects were associated with increases in protein levels and/or activation of canonical angiogenesis pathway associated events (HIF1a, VEGF, VEGFR2, PI3K, PDK, AKT, eNOS, NO, cGMP, MMP-2/-9, Src-1, and CD31). Thus, the use of Epi may represent a safe and novel means to stimulate myocardial angiogenesis.

The purpose of this study was to determine whether (-)-epicatechin (mainly found in cocoa) could attenuate detraining effects in the hindlimb muscles of mice. Thirty-two male mice were randomized into 4 groups: control, trained, trained with 14 d of detraining and vehicle (DT-14-W), and trained with 14 d of detraining and (-)-epicatechin [DT-14-(-)-Epi]. DT-14-(-)-Epi received (-)-epicatechin (1.0 mg/kg 2 &times;/d), whereas water was given to the DT-14-W group. The latter 3 groups performed 5 wk of endurance training 5 &times;/wk. Hindlimb muscles were harvested, and Western blots, as well as enzyme analyses, were performed. Training significantly increased capillary-to-fiber ratio (≈ 78.8%), cytochrome-c oxidase (≈ 35%), and activity (≈ 144%) compared to controls. These adaptations returned to control levels for the DT-14-W group, whereas the DT-14-(-)-Epi group was able to maintain capillary-to-fiber ratio (≈ 44%), CcO protein expression (≈ 45%), and activity (≈ 108%) above control levels. In addition, the increase in capillarity was related to decreased protein expression of thrombospondin-1, an antiangiogenic regulator. Furthermore, there were no significant differences in endurance capacity between the trained and DT-14-(-)-Epi groups. Our data suggest that (-)-epicatechin may be a suitable compound to maintain exercise-induced improved capillarity and mitochondrial capacity, even when exercise regimens are discontinued.

Recovery from skeletal muscle injury is often incomplete because of the formation of fibrosis and inadequate myofiber regeneration; therefore, injured muscle could benefit significantly from therapies that both stimulate muscle regeneration and inhibit fibrosis. To this end, we focused on blocking myostatin, a member of the transforming growth factor-β superfamily and a negative regulator of muscle regeneration, with the myostatin antagonist follistatin. In vivo, follistatin-overexpressing transgenic mice underwent significantly greater myofiber regeneration and had less fibrosis formation compared with wild-type mice after skeletal muscle injury. Follistatin's mode of action is likely due to its ability to block myostatin and enhance neovacularization. Furthermore, muscle progenitor cells isolated from follistatin-overexpressing mice were significantly superior to muscle progenitors isolated from wild-type mice at regenerating dystrophin-positive myofibers when transplanted into the skeletal muscle of dystrophic mdx/severe combined immunodeficiency mice. In vitro, follistatin stimulated myoblasts to express MyoD, Myf5, and myogenin, which are myogenic transcription factors that promote myogenic differentiation. Moreover, follistatin's ability to enhance muscle differentiation is at least partially due to its ability to block myostatin, activin A, and transforming growth factor-β1, all of which are negative regulators of muscle cell differentiation. The findings of this study suggest that follistatin is a promising agent for improving skeletal muscle healing after injury and muscle diseases, such as the muscular dystrophies.

Hey Brundel!! I'm brand new to this site but have been researching for years on here for various products/recommendations. I'm an ex-NFL athlete. I have absolutely 0% knowledge about the steroid/PH side of supplements. But I do know how to train at a very high level. It's obvious you know exactly what you are talking about. I have a few questions if you would be kind enough to answer them.
1. When will the new Follidrone be available and how fast can I get it?
2. I recently ordered Formeron but have yet to use it. If I want to gain good clean mass, what is the best PH to stack with it? I'm totally oblivious to this so I need complete direction like you are teaching a baby to walk lol. I would like something fairly safe that won't destroy my liver, though I know it's give and take with everything. Hope all is well, thank you in advance.

Hey Brundel!! I'm brand new to this site but have been researching for years on here for various products/recommendations. I'm an ex-NFL athlete. I have absolutely 0% knowledge about the steroid/PH side of supplements. But I do know how to train at a very high level. It's obvious you know exactly what you are talking about. I have a few questions if you would be kind enough to answer them.
1. When will the new Follidrone be available and how fast can I get it?
2. I recently ordered Formeron but have yet to use it. If I want to gain good clean mass, what is the best PH to stack with it? I'm totally oblivious to this so I need complete direction like you are teaching a baby to walk lol. I would like something fairly safe that won't destroy my liver, though I know it's give and take with everything. Hope all is well, thank you in advance.

Hey bud

Follidrone will be available for Pre sale at another vendor Who I wont promote here out of respect for Orbit. You can PM me if you like.
Otherwise Orbit should have it by the 15th approximately.

If it were me ( I cant give medication advice) I would personally use 500mg injected testosterone cypionate for 10 weeks with a post cycle therapy starting 3 weeks after last injection and consisting of 50mg clomid per day and 1-2 pumps Formeron per day for 4 weeks total.

Thanks so much for replying! If it were you, what would you stack with the EpiTren? I would ask you this in PM but I'm still trying to figure out how to work this from my phone lol, I'm trying to see how to upload an avatar pic too